Estimates of global, regional, and national incidence, prevalence, and mortality of HIV, 1980-2015: the Global Burden of Disease Study 2015

Timely assessment of the burden of HIV/AIDS is essential for policy setting and programme evaluation. In this report from the Global Burden of Disease Study 2015 (GBD 2015), we provide national estimates of levels and trends of HIV/AIDS incidence, prevalence, coverage of antiretroviral therapy (ART), and mortality for 195 countries and territories from 1980 to 2015.For countries without high-quality vital registration data, we estimated prevalence and incidence with data from antenatal care clinics and population-based seroprevalence surveys, and with assumptions by age and sex on initial CD4 distribution at infection, CD4 progression rates (probability of progression from higher to lower CD4 cell-count category), on and off antiretroviral therapy (ART) mortality, and mortality from all other causes. Our estimation strategy links the GBD 2015 assessment of all-cause mortality and estimation of incidence and prevalence so that for each draw from the uncertainty distribution all assumptions used in each step are internally consistent. We estimated incidence, prevalence, and death with GBD versions of the Estimation and Projection Package (EPP) and Spectrum software originally developed by the Joint United Nations Programme on HIV/AIDS (UNAIDS). We used an open-source version of EPP and recoded Spectrum for speed, and used updated assumptions from systematic reviews of the literature and GBD demographic data. For countries with high-quality vital registration data, we developed the cohort incidence bias adjustment model to estimate HIV incidence and prevalence largely from the number of deaths caused by HIV recorded in cause-of-death statistics. We corrected these statistics for garbage coding and HIV misclassification.Global HIV incidence reached its peak in 1997, at 3·3 million new infections (95% uncertainty interval [UI] 3·1-3·4 million). Annual incidence has stayed relatively constant at about 2·6 million per year (range 2·5-2·8 million) since 2005, after a period of fast decline between 1997 and 2005. The number of people living with HIV/AIDS has been steadily increasing and reached 38·8 million (95% UI 37·6-40·4 million) in 2015. At the same time, HIV/AIDS mortality has been declining at a steady pace, from a peak of 1·8 million deaths (95% UI 1·7-1·9 million) in 2005, to 1·2 million deaths (1·1-1·3 million) in 2015. We recorded substantial heterogeneity in the levels and trends of HIV/AIDS across countries. Although many countries have experienced decreases in HIV/AIDS mortality and in annual new infections, other countries have had slowdowns or increases in rates of change in annual new infections.Scale-up of ART and prevention of mother-to-child transmission has been one of the great successes of global health in the past two decades. However, in the past decade, progress in reducing new infections has been slow, development assistance for health devoted to HIV has stagnated, and resources for health in low-income countries have grown slowly. Achievement of the new ambitious goals for HIV enshrined in Sustainable Development Goal 3 and the 90-90-90 UNAIDS targets will be challenging, and will need continued efforts from governments and international agencies in the next 15 years to end AIDS by 2030.Bill & Melinda Gates Foundation, and National Institute of Mental Health and National Institute on Aging, National Institutes of Health

Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015

BACKGROUND: The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. METHODS: We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors-the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI). FINDINGS: Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%. Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period. All risks jointly evaluated in 2015 accounted for 57·8% (95% CI 56·6-58·8) of global deaths and 41·2% (39·8-42·8) of DALYs. In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]). From 1990 to 2015, attributable DALYs declined for micronutrient deficiencies, childhood undernutrition, unsafe sanitation and water, and household air pollution; reductions in risk-deleted DALY rates rather than reductions in exposure drove these declines. Rising exposure contributed to notable increases in attributable DALYs from high BMI, high fasting plasma glucose, occupational carcinogens, and drug use. Environmental risks and childhood undernutrition declined steadily with SDI; low physical activity, high BMI, and high fasting plasma glucose increased with SDI. In 119 countries, metabolic risks, such as high BMI and fasting plasma glucose, contributed the most attributable DALYs in 2015. Regionally, smoking still ranked among the leading five risk factors for attributable DALYs in 109 countries; childhood underweight and unsafe sex remained primary drivers of early death and disability in much of sub-Saharan Africa. INTERPRETATION: Declines in some key environmental risks have contributed to declines in critical infectious diseases. Some risks appear to be invariant to SDI. Increasing risks, including high BMI, high fasting plasma glucose, drug use, and some occupational exposures, contribute to rising burden from some conditions, but also provide opportunities for intervention. Some highly preventable risks, such as smoking, remain major causes of attributable DALYs, even as exposure is declining. Public policy makers need to pay attention to the risks that are increasingly major contributors to global burden

Effect of Ephedra alata Decne. on lipids metabolism of Aspergillus flavus Link

In Aspergillus flavus Link, the total lipid, sterols, neutral lipids, phospholipids and fatty acid content decreased significantly with the application of different concentrations of Ephedra alata Decne. extrtact. Gas chromatographic analysis revealed the presence of 12 fatty acids namely, (caprylic (C8), capric (C10), lauric (C12), myristic (C14), palmitic (C16), palmitoleic (C16:1), stearic (C18), oleic (C18:1), linoleic (C18:2), ? linolenic (C18:3), arachidic (C20) and arachidonic (C20:4) with total un-saturation per cent 69.78 in the cellular lipids of A. flavus. The use of E. alata extracts induced significant alteration in fatty acid profile towards increment saturation. DOI: http://dx.doi.org/10.3329/bjb.v42i1.15823 Bangladesh J. Bot. 42(1): 45-49, 2013 (June)</jats:p

Plant growth regulators improve the yield of white lupin (Lupinus albus) by enhancing the plant morpho-physiological functions and photosynthesis under salt stress

ABSTRACT Background: White lupin (Lupinus albus L.) is a multi-purpose, climate resilient, pulse crop with exceptionally high protein content that makes it a suitable alternative of soybean in livestock feed. Although white lupin grows well on marginal sandy soils, previous studies have reported its sensitivity towards salinity stress. This experiment aims to assess the influence of salinity stress and mitigating role of plant growth regulators (PGRs) on performance of white lupin.  Methodology: The white lupin plants were sown in pots maintained at three salinity levels (1, 3 and 4.5 dS m− 1) throughout the growing season and foliar sprayed with different PGRs, including ascorbic acid, potassium chloride, boric acid, ammonium molybdate and methionine at sowing, four weeks after emergence and at the initiation of flowering. Foliar spray of distilled water and salinity level of 1 dS m− 1 were maintained as control treatments. Data were recorded for seed germination indices, plant growth, antioxidant enzymes and photosynthetic efficiency variables.  Results: The severe salinity stress (4.5 dS m− 1) reduced the germination indices by 9–50%, plant growth traits by 26–54%, root nodulation by 12–26%, grain development by 44–53%, antioxidant enzymes activity by 13–153% and photosynthetic attributes by 1–8% compared to control (1 dS m− 1). Different PGRs improved several morpho-physiological attributes in a varied manner. The application of potassium chloride improved seed vigour index by 53%, while ascorbic acid improved root nodulation by 12% and number of pods per cluster by 75% at the severe salinity level. The foliar application of PGRs also displayed a recovery of 140% in the activity of superoxide dismutase and 70% in catalase. The application of multi zinc displayed an improvement of 37% in plant relative chlorophyll, while ascorbic acid brought an increase of 25% in non-photochemical quenching and 21% in photochemical quenching coefficient at the severe salinity level. On contrary, the application of PGRs brought a relatively modest improvement (8–13%) in quantum yield of photosystem II at slight to moderate (3 dS m− 1) salinity stress. The correlation analysis confirmed a partial contribution of leaf area and seed vigour index to overall photosynthetic efficiency of white lupin.  Conclusions: Clearly, salinity exerted a negative impact on white lupin through a decline in chlorophyll content, activity of antioxidant enzymes and efficiency of photosynthetic apparatus. However, PGRs, especially ascorbic acid and potassium chloride considerably improved white lupin growth and development by mitigating the negative effects of salinity stress.</p

Black root rot: a long known but little understood disease

Table S1. Hosts reported to be susceptible to black root rot infection.Table S2. Variation in host susceptibility to black root rot infection by the fungus formally known as Thielaviopsis basicola.Black root rot caused by the pathogen Thielaviopsis basicola has been known since the mid 1800s. The disease is important on many agricultural and ornamental plant species and has been found in at least 31 countries. Since its description, the pathogen has had a complex taxonomic history that has resulted in a confused literature. A recent revision of the Ceratocystidaceae following the advent of DNA sequencing technology has made it possible to resolve this confusion. Importantly, it has also shown that there are two pathogens in the Ceratocystidaceae that cause black root rot. They reside in the newly established genus Berkeleyomyces and are now known as B. basicola and B. rouxiae. This review considers the taxonomic history of the black root rot pathogens, and their global distribution. Prospects relating to the serious diseases that they cause and the likely impact that the era of genomics will have on our understanding of the pathogens are also highlighted.The University of Pretoria, the members of Tree Protection Co‐operative Programme (TPCP), the DST‐NRF Centre of Excellence in Tree Health Biotechnology (CTHB) and the National Research Foundation.https://onlinelibrary.wiley.com/journal/136530592020-06-01hj2019BiochemistryForestry and Agricultural Biotechnology Institute (FABI)GeneticsMicrobiology and Plant Patholog